NeuroTalk Support Groups - View Single Post - A word of caution about caffeine/nightshades

mrsD · 03-10-2009, 01:56 PM

I found this post yesterday, and thought I would do some research on it.

Let me start with Mestinon. This drug has been around for about 40 years. When it came out, back then, research was not what it is today.

For example. Pyridostigmine has been used in NORMAL humans to try and block the actions of poison gases during war.

Quote:

Vet Hum Toxicol. 1997 Aug;39(4):214-9.Links
Potentiation of pyridostigmine bromide toxicity in mice by selected adrenergic agents and caffeine.
Chaney LA, Rockhold RW, Mozingo JR, Hume AS, Moss JI.

Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, USA.

Pyridostigmine bromide (PB) is a reversible cholinesterase inhibitor used routinely in the treatment of myasthenia gravis and recently by the US Army as a prophylactic agent against potential nerve gas attack in the Persian Gulf War. Pyridostigmine has been implicated as one of several possible causative factors associated with Persian Gulf illnesses. To investigate toxic interactions between PB and other drugs, male ICR mice received contralateral ip injections of either a selected adrenergic drug or caffeine, followed 15 min later by PB. Representative isobolograms plotted for each drug interaction illustrate that a beta-adrenoceptor agonist (isoproterenol), selective beta 2-adrenoceptor agonists (salbutamol, terbutaline), alpha 1- and alpha 2-adrenoceptor antagonists (yohimbine, phentolamine, prazosin), as well as the stimulant caffeine, strongly potentiate the lethal effect of PB. Agents with agonist activity at both alpha- and beta-adrenoceptors (epinephrine, norepinephrine) additively increase PB-induced lethality. The potentiation of toxicity between PB and these agents was counteracted by pretreatment with atropine and atropine methyl nitrate. An alpha 2-adrenoceptor agonist (clonidine) and beta-adrenoceptor antagonists (propranolol, nadolol, acebutolol) did not increase PB-induced lethalities. These data demonstrate a toxic synergism between PB, several commonly used classes of adrenergic agents and caffeine when exposure occurs in different combinations. Future studies into the mechanism(s) of these interactions may bring into question the usage of PB as a protective agent in combat conditions as well as delineate any possible contributions of the drug to Persian Gulf illnesses.

PMID: 9251170 [PubMed - indexed for MEDLINE]

from http://www.ncbi.nlm.nih.gov/sites/en...h&term=9251170

What this means is that normal mice (those without a lack of acetylcholine), suffered lethal results when given both pyridostigmine and drugs I bolded in the abstract.
Tests were not done on humans, obviously, and I think this is hard to extrapolate to MG patients. So don't become alarmed yet about the word "lethal" as used here.

This is a pretty good article about MG as we know it today.
http://74.125.47.132/search?q=cache:...nk&cd=10&gl=us
This is a 2005 CE about MG and its treatment.
The mention of caffeine about 1/2 way down the lesson:

Quote:

Several drugs increase the force of responses within single muscle fibers. In those fibers that can respond, the muscle action potential is prolonged. Caffeine and ephedrine exhibit this activity. Unfortunately, the response of the muscle requires a contraction rather than a twitch effect. Therefore, these drugs are not very beneficial......

Now the Nightshade family of vegetables.
I find this an interesting subject, as I have found that potatoes set off my arthritis and PN symptoms. So I have been avoiding them for over a year. A reintroduction of a modest serving will give me symptoms again.

I found some interesting articles on this:

Quote:

Anesthesiology. 2000 Aug;93(2):510-9.Click here to read Links
Cholinesterase inhibition by potato glycoalkaloids slows mivacurium metabolism.
McGehee DS, Krasowski MD, Fung DL, Wilson B, Gronert GA, Moss J.

Department of Anesthesia and Critical Care and the Committee on Neurobiology, University of Chicago, IL 60637, USA.

BACKGROUND: The duration of action for many pharmaceutical agents is dependent on their breakdown by endogenous hydrolytic enzymes. Dietary factors that interact with these enzyme systems may alter drug efficacy and time course. Cholinesterases such as acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) hydrolyze and inactivate several anesthetic drugs, including cocaine, heroin, esmolol, local ester anesthetics, and neuromuscular blocking drugs. Natural glycoalkaloid toxins produced by plants of the family Solanaceae, which includes potatoes and tomatoes, inhibit both AChE and BuChE. Here the authors assess the extent to which two solanaceous glycoalkaloids (SGAs), alpha-solanine and alpha-chaconine, can alter the effects of neuromuscular blocking drugs and cholinesterase inhibitors in vivo and in vitro. METHODS: Inhibition of purified human AChE and BuChE by SGAs, neuromuscular blocking drugs, and cholinesterase inhibitors was assessed by an in vitro colorimetric cholinesterase assay. In vivo experiments were carried out using anesthetized rabbits to test whether SGAs affect recovery from mivacurium-induced paralysis. RESULTS: SGAs inhibited human BuChE at concentrations similar to those found in serum of individuals who have eaten a standard serving of potatoes. Coapplication of SGAs (30-100 nm) with neuromuscular blocking drugs and cholinesterase inhibitors produced additive cholinesterase inhibition. SGA administration to anesthetized rabbits inhibited serum cholinesterase activity and mivacurium hydrolysis. In addition, SGA prolonged the time needed for recovery from mivacurium-induced paralysis (149 +/- 12% of control; n = 12). CONCLUSIONS: These findings support the hypothesis that inhibition of endogenous enzyme systems by dietary factors can influence anesthetic drug metabolism and duration of action. Diet may contribute to the wide variation in recovery time from neuromuscular blockade seen in normal, healthy individuals.

PMID: 10910502 [PubMed - indexed for MEDLINE]

from http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

So what do these studies show? That under certain conditions the alkaloids in potatoes may exert an increased recovery time to normal people who have been given a
mivacurium-induced paralysis (during a medical procedure).
Would this be additive to a drug like Mestinon?
That is really hard to say.
In the 40 years Mestinon has been around (granted not used heavily due to the uncommon incidence of MG), but still we would have some anecdotal reports at PubMed on using it with certain foods or coffee tea.

I could not find any warnings in the professional literature on food intake with Mestinon. None of the drug checkers have an interaction posted with caffeine.

The nightshade vegetables have very reduced levels of alkaloids (mostly solanine) in the fruit/tubers. The majority of the alkaloids reside in the green leafy structures which we do not eat. Potatoes do have that green tint in the skin, which many know can cause GI upset when eaten, whether one has MG or not.

So certainly you can ask your neurologist about this connection with foods/coffee and the use of Mestinon. I wouldn't worry however about chocolate at this time.